How age changes affect the cellular kinetic behavior of skeletal tissues during growth, development, remodeling and repair is a basic question of paramount importance. To this end studies have been designed to determine age changes in the cellular and matrical complement of skeletal-dental tissues in both normal and injured short-lived mice as the experimental model. A variety of techniques encompassing morphological, autoradiographic and histo-cytochemical methods at light-microscopic, as well as, micron-microscopic levels are used. In order to develop a better understanding of changes in the cellular proliferative kinetic, cellular behavior and repair potentials of aging skeletal cell systems, radioactive tracers are employed, such as tritiated thymidine, tritiated uridine, tritiated amino acids and tritiated carbohydrates. The data collected and knowledge gained from these studies will serve as a base line for a wide variety of future undertakings devoted to assessing the response and behavior of bone to perturbations such as radiation injury, nutrition and hormonal variations, and physical, chemical and bacterial trauma, concomitant with aging. Collectively, these studies have produced the most detailed biological account of tissue degenerative events leading to senile atrophy of bone and to the loss of cellular control and biofeedback important to mineral homeostasis. BIBLIOGRAPHIC REFERENCES: Tonna, E.A., and Singh, I.J.: An autoradiographic investigation of 3H-uridine utilization by aging mouse cartilage cells. Exper. Gerontol., 11: 231-241, 1977. Tonna, E.A.: Aging of skeletal-dental systems and supporting tissues. In The Handbook of the Biology of Aging, J.E. Birren (ed.), Chapt. 18, Van Nostrand Co., New York (in press), 1977.